Hypophosphatem ia

GENERAL PRINCIPLES

• A serum phosphate 100 mg by 24-hour urine collection or a fractional excretion of phosphate >5% during hypophosphatemia indicates excessive renal loss.

• Low serum 25(OH)D₃ suggests dietary vitamin D deficiency or malabsorption.

TREATMENT

• Acute moderate hypophosphatemia (1.0-2.5 mg/dL) is common in the hospitalized patient and is often due simply to transcellular shifts, requiring no treatment if asymptomatic, except correction of the underlying cause.

• Acute severe hypophosphatemia (2.2 mEq/L defines hypermagnesemia.

• Most cases of clinically significant hypermagnesemia are iatrogenic, occurring with large doses of magnesium-containing antacids or laxatives and during treatment of preeclampsia with IV magnesium. Because renal excretion is the only means of lowering serum magnesium levels, the presence of significant renal insufficiency can lead to magnesium toxicity even with therapeutic doses of these antacids and laxatives.

• Mild, insignificant elevations in magnesium can occur in end-stage renal disease patients, theophylline intoxication, DKA, and tumor lysis syndrome.

DIAGNOSIS

Clinical Presentation

• Signs and symptoms are usually seen when the serum magnesium level is >4 mEq/L.

• Neuromuscular abnormalities usually include hyporeflexia (usually the first sign of magnesium toxicity), lethargy, and weakness that can progress to paralysis and diaphragmatic involvement, leading to respiratory failure.

• Cardiac findings include hypotension, bradycardia, and cardiac arrest.

Diagnostic Testing

The ECG may reveal bradycardia and prolonged PR, QRS, and QT intervals with magnesium levels of 5-10 mEq/L. Complete heart block or asystole may eventually ensue with levels >15 mEq/L.

TREATMENT

• Prevention. In the setting of significant renal insufficiency, the inadvertent administration of magnesium-containing medications (e.g., Maalox, magnesium citrate) should be avoided.

• Asymptomatic hypermagnesemia. In the setting of normal renal function, normal magnesium levels will quickly be attained with removal of the magnesium load.

• Symptomatic hypermagnesemia

î Prompt supportive therapy is critical, including mechanical ventilation for respiratory failure and a temporary pacemaker for significant bradyarrhythmias.

î The effects of hypermagnesemia can be antagonized quickly by the administration of 10% calcium gluconate 10-20 mL IV (1-2 g) over 10 minutes.

î Renal excretion can be encouraged with saline administration. With significant renal insufficiency, hemodialysis is required for definitive therapy.